|ZFIN ID: ZDB-PUB-141230-16|
Decreased anti-regenerative effects after spinal cord injury in spry4-/- mice
Goldshmit, Y., Frisca, F., Kaslin, J., Pinto, A.R., Tang, J.K., Pébay, A., Pinkas-Kramarski, R., Currie, P.D.
|Source:||Neuroscience 287: 104-12 (Journal)|
|Registered Authors:||Currie, Peter D., Goldshmit, Yona, Kaslin, Jan, Pinto, Andreia|
|Keywords:||Spry4-/- astrocytes inflammationspinal cord injury|
|PubMed:||25541251 Full text @ Neuroscience|
Goldshmit, Y., Frisca, F., Kaslin, J., Pinto, A.R., Tang, J.K., Pébay, A., Pinkas-Kramarski, R., Currie, P.D. (2015) Decreased anti-regenerative effects after spinal cord injury in spry4-/- mice. Neuroscience. 287:104-12.
ABSTRACTPreviously, we have demonstrated a role for Fgf in spinal cord regeneration in both zebrafish and mouse. We have shown that exogenous Fgf2 treatment attenuates astrocytic gliosis and induces glia cells to become progenitors that undergo neurogenesis as well as differentiating into bipolar astrocytes that support axonal regeneration (Goldshmit et al., 2014; Goldshmit et al., 2012). One of the downstream signalling target genes of Fgf is spry4, which acts as a feedback inhibitor for Fgf signalling. In this study we examined the effects of increased endogenous Fgf signalling, in spry4-/- mice, on the early events that occur after spinal cord injury. We demonstrate that in spry4-/- mice inflammatory responses, such as TNFα secretion and macrophage/neutrophil invasion into the lesion site are reduced. In addition, astrocytic gliosis is attenuated and neuronal survival is increased. These results further support a pro-regenerative role of Fgf after spinal cord injury, and suggest that increased endogenous Fgf signalling after spinal cord injury may contribute to functional recovery and therefore presents this pathway as a target for new therapy development.
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